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. 2013 Jul 30;305(8):E1007–E1017. doi: 10.1152/ajpendo.00063.2013

Fig. 6.

Fig. 6.

Liver-specific Gcn2 KO (LiGcn2 KO) mice and Gcn2-deficient primary hepatocytes display misregulation of gluconeogenesis. A: blood glucose levels as a function of time after ip injection of sodium pyruvate in LiGcn2 KO and WT mice after 24 h fasting (mean ± SE, n ≥ 6; P = 0.003, KO vs. WT by 2-way ANOVA). B: expression of Cebpβ, G6pc, and Pepck mRNAs in livers of LiGcn2 KO and WT mice after 24 h fasting (normalized to fed WT mice, mean ± SE, n = 4; *P < 0.05 as indicated). C: glucose production of primary Gcn2 KO and WT hepatocytes in glucose production medium supplemented with sodium pyruvate and cAMP or control medium (mean ± SE, n ≥ 4; *P < 0.05 as indicated). D: expression of Pepck, G6pc, Pgc1α, and Cebpβ mRNAs in primary Gcn2 KO and WT hepatocytes in glucose production assay (normalized to control group, mean ± SE, n = 4; *P < 0.05 as indicated). E: expression of CEBPβ mRNA in livers of fed and 24-h-fasted WT and Gcn2 KO mice (normalized to fed WT mice, mean ± SE, n = 8; *P < 0.05 as indicated). F: C/EBPβ (LAP) protein from liver lysates of fed and 24-h-fasted mice of indicated genotypes. Top, Western blot; bottom, CEBPβ protein relative to tubulin (mean ± SE, n = 3; *P < 0.05 as indicated).